Transcriptional landscape of trans-kingdom communication between Candida albicans and Streptococcus gordonii

LC Dutton, KH Paszkiewicz, RJ Silverman, PR Splatt, S Shaw, AH Nobbs, RJ Lamont, HF Jenkinson (Corresponding Author), M Ramsdale

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)

Abstract

Recent studies have shown that the transcriptional landscape of the pleiomorphic fungus Candida albicans is highly dependent upon growth conditions. Here using a dual RNA‐seq approach we identified 299 C. albicans and 72 Streptococcus gordonii genes that were either upregulated or downregulated specifically as a result of co‐culturing these human oral cavity microorganisms. Seventy‐five C. albicans genes involved in responses to chemical stimuli, regulation, homeostasis, protein modification and cell cycle were significantly (P ≤ 0.05) upregulated, whereas 36 genes mainly involved in transport and translation were downregulated. Upregulation of filamentation‐associated TEC1 and FGR42 genes, and of ALS1 adhesin gene, concurred with previous evidence that the C. albicans yeast to hypha transition is promoted by S. gordonii. Increased expression of genes required for arginine biosynthesis in C. albicans was potentially indicative of a novel oxidative stress response. The transcriptional response of S. gordonii to C. albicans was less dramatic, with only eight S. gordonii genes significantly (P ≤ 0.05) upregulated at least two‐fold (glpK, rplO, celB, rplN, rplB, rpsE, ciaR and gat). The expression patterns suggest that signals from S. gordonii cause a positive filamentation response in C. albicans, whereas S. gordonii appears to be transcriptionally less influenced by C. albicans.
Original languageEnglish
Pages (from-to)131-161
Number of pages31
JournalMolecular Oral Microbiology
Volume31
Issue number2
Early online date7 Jul 2015
DOIs
Publication statusPublished - Apr 2016

Bibliographical note

Funding: NIH (NIDCR), Bethesda. Grant Number: R01DE016690

Keywords

  • adhesin
  • bacteria-fungi interactions
  • cell wall proteins
  • GPI anchor
  • RNA-Seq

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